Obstructive sleep apnea occurs when the upper airway repeatedly collapses during sleep, causing breathing cessation (apneas) or airflow limitation (hypopneas). Each event triggers a brief arousal from sleep and a sympathetic surge as the brain restores breathing. The apnea-hypopnea index (AHI) quantifies severity: mild is 5–14 events/hour, moderate is 15–29, severe is ≥30. A patient with severe OSA may have their breathing disrupted hundreds of times per night, each time activating the stress response.
The cardiovascular consequences of untreated OSA are substantial. The intermittent hypoxia and nocturnal sympathetic activation produce chronic hypertension, atrial fibrillation, pulmonary hypertension, increased risk of myocardial infarction and stroke, and accelerated atherosclerosis. OSA is an independent risk factor for cardiovascular mortality. In patients with treatment-resistant hypertension, undiagnosed OSA is one of the most common identifiable causes.
Diagnosis requires sleep testing — either in-lab polysomnography or, more commonly now, home sleep apnea testing (HSAT). HSATs are validated, accessible, and appropriate for most adults with suspected uncomplicated OSA. They measure AHI and oxygen saturation but do not capture sleep staging — patients with complex sleep disorders, central apnea, or significant comorbidities warrant in-lab testing.
CPAP (continuous positive airway pressure) remains the gold standard treatment. It works as a pneumatic splint, maintaining positive pressure throughout the airway. Adherence is the challenge — most guidelines define adherence as ≥4 hours/night on ≥70% of nights. CPAP alternatives include oral appliances (for mild-moderate OSA or CPAP-intolerant patients), hypoglossal nerve stimulation (Inspire device), and positional therapy for position-dependent OSA.